Acutely Decompensated Heart Failure

February 2002Volume 4, Number 2

Authors

Joshua M. Kosowsky, MDDepartment of Emergency Medicine, Brigham andWomen’s Hospital, Boston, MA.

Leo Kobayashi, MDDepartment of Emergency Medicine, Brigham andWomen’s Hospital, Boston, MA.

Peer Reviewers

Francis M. Fesmire, MDDirector, Heart-Stroke Center, Chattanooga, TN.

Christopher J. Rosko, MD, FACEPMedical Director, Department of EmergencyMedicine, University of Alabama at Birmingham,Birmingham, AL.

CME Objectives

Upon completing this article, you should be able to:1. describe the basic pathophysiology of acutely

decompensated heart failure;2. identify the common and life-threatening

precipitants of acutely decompensatedheart failure;

3. explain the management of acutelydecompensated heart failure in the prehospitaland ED settings, including the role ofdiuretics, vasodilators, inotropes, andnoninvasive ventilatory support; and

4. describe the role of risk stratification indetermining the disposition of patients withacutely decompensated heart failure.

Date of original release: February 1, 2002.Date of most recent review: January 18, 2002.

See “Physician CME Information” on back page.

EMERGENCY MEDICINE PRACTICEA N E V I D E N C E - B A S E D A P P R O A C H T O E M E R G E N C Y M E D I C I N E

Editor-in-Chief

Stephen A. Colucciello, MD, FACEP,Assistant Chair, Director ofClinical Services, Department ofEmergency Medicine, CarolinasMedical Center, Charlotte, NC;Associate Clinical Professor,Department of EmergencyMedicine, University of NorthCarolina at Chapel Hill, ChapelHill, NC.

Associate Editor

Andy Jagoda, MD, FACEP, Professorof Emergency Medicine; Director,International Studies Program,Mount Sinai School of Medicine,New York, NY.

Editorial Board

Judith C. Brillman, MD, ResidencyDirector, Associate Professor,Department of EmergencyMedicine, The University of

New Mexico Health SciencesCenter School of Medicine,Albuquerque, NM.

W. Richard Bukata, MD, AssistantClinical Professor, EmergencyMedicine, Los Angeles County/USC Medical Center, Los Angeles,CA; Medical Director, EmergencyDepartment, San Gabriel ValleyMedical Center, San Gabriel, CA.

Francis M. Fesmire, MD, FACEP,Director, Chest Pain—StrokeCenter, Erlanger Medical Center;Assistant Professor of Medicine,UT College of Medicine,Chattanooga, TN.

Valerio Gai, MD, Professor and Chair,Department of EmergencyMedicine, University of Turin, Italy.

Michael J. Gerardi, MD, FACEP,Clinical Assistant Professor,Medicine, University of Medicineand Dentistry of New Jersey;Director, Pediatric EmergencyMedicine, Children’s MedicalCenter, Atlantic Health System;

Vice-Chairman, Department ofEmergency Medicine, MorristownMemorial Hospital.

Michael A. Gibbs, MD, FACEP,Residency Program Director;Medical Director, MedCenter Air,Department of EmergencyMedicine, Carolinas MedicalCenter; Associate Professor ofEmergency Medicine, Universityof North Carolina at Chapel Hill,Chapel Hill, NC.

Gregory L. Henry, MD, FACEP,CEO, Medical Practice RiskAssessment, Inc., Ann Arbor,MI; Clinical Professor, Departmentof Emergency Medicine, Universityof Michigan Medical School, AnnArbor, MI; President, AmericanPhysicians Assurance Society, Ltd.,Bridgetown, Barbados, West Indies;Past President, ACEP.

Jerome R. Hoffman, MA, MD, FACEP,Professor of Medicine/Emergency Medicine, UCLASchool of Medicine; Attending

Physician, UCLA EmergencyMedicine Center; Co-Director,The Doctoring Program,UCLA School of Medicine,Los Angeles, CA.

John A. Marx, MD, Chair and Chief,Department of EmergencyMedicine, Carolinas MedicalCenter, Charlotte, NC; ClinicalProfessor, Department ofEmergency Medicine, Universityof North Carolina at Chapel Hill,Chapel Hill, NC.

Michael S. Radeos, MD, MPH, FACEP,Attending Physician inEmergency Medicine, LincolnHospital, Bronx, NY; ResearchFellow in Emergency Medicine,Massachusetts General Hospital,Boston, MA; Research Fellow inRespiratory Epidemiology,Channing Lab, Boston, MA.

Steven G. Rothrock, MD, FACEP, FAAP,Associate Professorof Emergency Medicine, Universityof Florida; Orlando Regional

Medical Center; Medical Director ofOrange County EmergencyMedical Service, Orlando, FL.

Alfred Sacchetti, MD, FACEP,Research Director, Our Lady ofLourdes Medical Center, Camden,NJ; Assistant Clinical Professorof Emergency Medicine,Thomas Jefferson University,Philadelphia, PA.

Corey M. Slovis, MD, FACP, FACEP,Department of EmergencyMedicine, Vanderbilt UniversityHospital, Nashville, TN.

Mark Smith, MD, Chairman,Department of EmergencyMedicine, Washington HospitalCenter, Washington, DC.

Charles Stewart, MD, FACEP,Colorado Springs, CO.

Thomas E. Terndrup, MD, Professorand Chair, Department ofEmergency Medicine, Universityof Alabama at Birmingham,Birmingham, AL.

Acutely DecompensatedHeart Failure: DiagnosticAnd Therapeutic StrategiesFor The New Millennium11 p.m.: You begin your shift. An elderly patient with shortness of breath has “CHF”written all over her. She looks and sounds “wet.” She gets the usual: oxygen, furo-semide, and nitrates. When you return 20 minutes later, she looks and feels much better.As you reach for the phone to speak with the admitting physician, you start to wonder,“Do I need to get cardiac enzymes? She really looks so good now—does she even need tobe admitted?”

ACUTELY decompensated heart failure is one of the most commoncardiac emergencies encountered in the ED. Because patients with heart

failure are seen so frequently, our evaluations can become perfunctory and ourtherapy homogenized. The fact is, patients with acutely decompensated heartfailure represent a diverse group that share common features, among them highmorbidity and mortality. Failure to appreciate and address the subtleties of anindividual exacerbation of heart failure can have dire consequences.

This issue of Emergency Medicine Practice presents a comprehensive,evidence-based approach to the management of acutely decompensated heartfailure. It focuses on the stabilization, differential diagnosis, pharmacologic andadjunctive therapies, and appropriate disposition of the individual patient.

Epidemiology, Etiology, And Definitions

As a result of the aging of the U.S. population, the overall prevalence of heartfailure is rising.1 At the same time, advances in outpatient medical therapy areallowing patients with chronic heart failure to survive despite advanced stagesof hemodynamic compromise. Nearly 5 million Americans have heart failure,and approximately 550,000 new cases arise each year.2 Heart failure nowaccounts for close to 1 million inpatient admissions annually and represents the

Emergency Medicine Practice 2 February 2002

number-one reason for hospitalization among the growingelderly population.2

Symptoms of decompensated heart failure commonlycause patients to seek emergency care. The NationalHospital Ambulatory Medical Care Survey reported 1.5million ED visits in 1999 for non-ischemic heart disease, ofwhich a significant proportion were related to heart failure.3

One retrospective analysis of 2 million ED visits over an 11-year period revealed approximately 1.1% of visits to have aprimary diagnosis of heart failure or pulmonary edema.4

Short-term outcomes for patients admitted to thehospital with decompensated heart failure have held fairlyconstant over the past two decades. In-hospital mortalityremains approximately 7%, with major adverse eventsoccurring in up to 18% of patients.5-7 For those patients whopresent with frank pulmonary edema, the correspondingrates of morbidity and mortality are approximatelydouble.8-11 Patients who present with acute myocardialinfarction and cardiogenic shock have a mortality rate of70% or more despite aggressive therapy.12 Less is knownabout the outcomes of patients who are sent home from theED. In a recent study of 112 patients discharged from the EDwith a primary diagnosis of heart failure, more than 60%experienced another ED visit, hospitalization, or deathwithin 90 days of the index visit.13

The etiologies of heart failure are numerous anddiverse. (See Table 1.) In the United States, the vast majorityof heart failure arises as a consequence of coronary arterydisease and/or long-standing hypertension. In the ED,acute heart failure can present de novo—for example, inacute myocardial infarction (MI) or with acute valvularinsufficiency. Much more commonly, patients seen in the EDhave chronic heart failure that has decompensated as theresult of one or more precipitating factors.

Chronic heart failure is a complex and multifacetedsyndrome with variable clinical presentations and overlap-ping systems of classification. Differentiating among thesecan be helpful in evaluating and managing individual

patients. Systolic failure is a physiologic state characterizedby impaired cardiac contractility—typically defined as anejection fraction less than 40%. In the case of diastolic failure,the ejection fraction is normal or supranormal, but myocar-dial relaxation is impaired, preventing proper filling ofthe ventricle.

Forward failure is a clinical constellation of symptomsrepresenting inadequate tissue perfusion, the extremeexample of which is cardiogenic shock. Pulmonary edema,peripheral edema, and congestive hepatomegaly distin-guish backward failure.

Right heart failure involves impaired return of blood tocentral venous circulation (as evidenced by neck veindistention, dependent extremity edema, and hepatomegaly).It is most commonly a consequence of severe left heart failurebut can also occur in isolation (as in the case of cor pulmon-ale) or result from right ventricular infarction. High-outputfailure is caused by excessive demand for tissue perfusionresulting in hyperdynamic cardiac dysfunction, as seen withsepsis, thyrotoxicosis, and beri-beri. Low output failure,distinguished by a low cardiac output, is the more commonpresentation of heart failure.

The severity of failure can be described in many ways,which may include a measure of how chronic failure affectsthe quality of life or more acute clinical parameters. Table 2on page 3 describes the new American Heart Associationclassification, the commonly used New York Heart Associa-tion (NYHA) classification, and the Killip classification(originally used to predict outcome after acute MI).

Pathophysiology

Regardless of etiology, inadequate cardiac function triggersa common set of compensatory mechanisms. These arebrought about by neurohormonal activation and character-ized by elevated sympathetic tone, fluid and salt retention,and ventricular remodeling. These adaptations can allowheart failure to remain stable (or “compensated”) for aperiod of time, but also provide the final common pathwayfor decompensation—a downward spiral resulting fromsome precipitant or stress.

High circulating levels of aldosterone, vasopressin,epinephrine, and norepinephrine are ultimately maladap-tive, as tachycardia and vasoconstriction compromise theperformance of the left ventricle (LV) and simultaneouslyworsen myocardial oxygen balance. Deteriorating leftventricular function results in further neurohormonalactivation and self-perpetuation of this adverse cycle. (SeeFigure 1 on page 3.)

Pathophysiologic considerations notwithstanding,acutely decompensated heart failure is a poorly definedclinical entity, and no universal definition exists.14 An acutedecompensation can develop over a period of minutes,hours, or days and can range in severity from mild symp-toms of volume overload or decreased cardiac output tofrank pulmonary edema or cardiogenic shock. However it isdefined, the number of heart failure patients who present tothe ED with clinical decompensation is likely to increaseover the coming years.

Table 1. Etiologies Of Heart Failure.

Coronary artery diseaseHypertensionValvular diseaseCardiomyopathy

• Idiopathic cardiomyopathy• Alcoholic cardiomyopathy• Toxin-related cardiomyopathy (e.g., adriamycin)• Postpartum cardiomyopathy• Hypertrophic obstructive cardiomyopathy (HOCM)• Tachyarrhythmia-induced cardiomyopathy

Infiltrative disorders (e.g., amyloid)Congenital heart diseasePericardial diseaseHyperkinetic states

• Anemia• Arteriovenous fistula• Thyroid disease• Beri-beri

3 Emergency Medicine PracticeFebruary 2002

State Of The Literature

Unfortunately, controlled trials provide few data to directthe optimal diagnosis and management of patients withacutely decompensated heart failure. In general, clinicaltrials have focused on heart failure arising in the context ofacute MI, although this subgroup represents 15% or fewer ofpatients hospitalized with heart failure.11,15 Much of theliterature on severely decompensated heart failure concernsthe management of patients after they have been admittedto the CCU. Care of patients in the ED—particularly forthose with mild-to-moderate symptoms—remains largely

empiric or based on observational studies and small case-series reports. The American College of Cardiology/American Heart Association (ACC/AHA) and the Agencyfor Health Care Policy and Research (AHCPR) havepublished practice guidelines that are based, in part, on theaforementioned literature.16,17

Differential Diagnosis

Decompensated heart failure can coexist with or closelymimic a number of other cardiac, respiratory, and systemicillnesses. (See Table 3 on page 4.) In fact, when patients

Table 2. Classifications Of Heart Failure.

American Heart Association Classification

Class DescriptionStage A Patients are at high risk for heart failure but have not developed structural heart disease and have no symptoms.Stage B Patients have developed structural heart disease but have not (yet) developed symptoms.Stage C Patients with past or current heart failure symptoms in association with structural damage to the heart.Stage D Patients with end-stage, or terminal, heart failure requiring specialized treatment strategies.

New York Heart Association Classification

Class Functional state SymptomsI No limitation Asymptomatic during usual daily activitiesII Slight limitation Mild symptoms (dyspnea, fatigue, or chest pain) with ordinary daily activitiesIII Moderate limitation Symptoms noted with minimal activityIV Severe limitation Symptoms at rest

Killip Classification

Class DescriptionKillip class I No evidence of pulmonary congestion or shock.Killip class II Mild pulmonary congestion (patients had rales up to 50% of each lung field ) or an isolated S3 gallop.Killip class III Pulmonary edema (rales more than 50% up).Killip class IV Hypotension and evidence of shock.

Sources: Hunt HA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executivesummary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the1995 Guidelines for the Evaluation and Management of Heart Failure). Circulation 2001;104: 2996-3007; and Killip T, Kimball JT. Treatment ofmyocardial infarction in coronary care unit. A two-year experience with 250 patients. Am J Cardiol 1967;20:457-467.

Figure 1. Heart Failure Pathophysiology Diagram.

symptomaticdecompensation

activation of renin-angiotensin systemactivation of sympathetic nervous system

cardiac ischemiadecreased left ventricle function

decreased cardiac outputincreased pulmonary capillary wedge pressure

increased heart rateincreased systemic vascular resistance

increased preload

➤

➤

➤

➤

➤


present to the ED with undifferentiated dyspnea, thediagnosis of heart failure is often overlooked.19 Patientswho present with mild or nonspecific symptoms posea particular diagnostic challenge. Symptoms such asweakness, lethargy, fatigue, anorexia, or lightheadednessmay actually be a manifestation of decreased cardiacoutput.20 Older patients frequently lack typical signs andsymptoms of heart failure.21 These features may be obscuredby the aging process itself or by the presence of coexistingmedical conditions.

Distinguishing heart failure from other life-threateningconditions may be as difficult as identifying its atypical orsubtle presentations. However, if an adequate history andphysical exam are not suggestive of heart failure, and both thechest radiograph and the ECG are normal, heart failure is unlikely.

Patients presenting with acute exacerbations of eithercardiac dysfunction or chronic obstructive pulmonarydisease (COPD) may have wheezing on pulmonaryauscultation with signs of chronic right-sided heart failure

and non-diagnostic chest radiographs. Bedside peak flowmeasurements may prove useful in these cases.22 In a studyof 56 acutely dyspneic patients, peak expiratory flow ratesof those with heart failure were found to be twice those ofpatients with COPD; however, no single cut-off provided forperfectly accurate classification.22 While ETCO2 levels forheart failure patients differ significantly from those ofasthma/COPD patients, once again, there is no singleETCO2 level that can reliably differentiate between the twoconditions.23 In heart failure patients, pulmonary embolismmay be clinically indistinguishable from an acute deteriora-tion of underlying failure.24

Precipitating factors for decompensation should besought in a careful and deliberate fashion. (See Table 4.)Ischemia/infarction and noncompliance with medicationsor dietary restrictions are the most common causes ofclinical decompensation.10,15,25-28 The exact prevalence of suchprecipitants varies depending on the particular population.Nevertheless, in almost all cases, the possibility of an acutecoronary syndrome should be considered. Other cardiovas-cular precipitants, such as arrhythmia, high-grade heartblock, severe valvular dysfunction, or hypertensive crisismust not be overlooked. It should also be recognized thatdecompensated heart failure can arise as a consequence ofnon-cardiac conditions such as sepsis, anemia, alcoholwithdrawal, uncontrolled diabetes, or thyroid disease.

“Out-worn heart, in a time out-worn,Come clear of the nets of wrong and right;Laugh, heart, again in the gray twilight.”

—William Butler Yeats (1865–1939), “Into the Twilight.”29

Prehospital Care

Even before patients reach the hospital, decompensatedheart failure is associated with significant morbidity andmortality, including malignant arrhythmias and prehospitalcardiac arrest.30 All patients should have continuous cardiacmonitoring and intravenous access established if possible.(See also “Clinical Pathway: Prehospital Therapy ForAcutely Decompensated Heart Failure” on page 13.)Because successful management depends on reversal ofhypoxia, pulse oximetry and supplemental oxygen shouldbe utilized routinely in the prehospital care of patients withdecompensated heart failure. Prehospital personnel shouldradio ED staff for any patient presenting with symptomssuggestive of pulmonary edema or cardiogenic shock andreceive on-line medical advice when appropriate.

The decision to treat a patient in the relatively uncon-trolled prehospital environment carries some risks that mustbe weighed against expected benefits. With few exceptions,the safety and efficacy of prehospital medications have beenpoorly studied.32 Prehospital therapy for decompensatedheart failure requires particular caution in light of therelatively high number of inaccurate diagnoses made in thefield. Nearly 30% of patients with respiratory distress(presumed in the field to be cardiac in origin) are diagnosedwith a different condition once they arrive at the hospi-tal.30,33,34 Despite these concerns, available evidence suggests

Table 4. Common Precipitants OfCHF Decompensation.

• Medication noncompliance• Dietary indiscretion• Uncontrolled hypertension• Myocardial ischemia/infarction• Acute valvular dysfunction• Cardiac arrhythmias• Pulmonary and other infections• Administration of inappropriate medications

(e.g., negative inotropes)• Fluid overload• Missed dialysis• Thyrotoxicosis• Anemia• Alcohol withdrawal

Table 3. Differential Diagnosis Of AcutelyDecompensated Heart Failure.

Cardiovascular• Acute myocardial infarction• Unstable angina• Acute valvular/septal rupture• Aortic dissection• Arrhythmia• Critical aortic stenosis• Endocarditis/myocarditis• Hypertensive crisis• Pericardial tamponade/effusion

Pulmonary• COPD• Pulmonary thromboembolism• Multilobar pneumonia• Acute respiratory distress syndrome (ARDS)

Other• Pure volume overload

• Renal failure• Iatrogenic (e.g., post-transfusion)

• Sepsis


that prehospital therapy for presumed heart failure canprevent serious complications and improve survival,particularly for critically ill patients.30,33,34 In Europeancountries, where physicians commonly staff ambulances,intensive prehospital treatment of patients with severe heartfailure confers short-term benefits.35,36

Sublingual nitroglycerin appears to be safest and mosteffective of the prehospital medications used for presumedpulmonary edema.33 Prehospital intravenous (IV) nitrates alsoyield positive short-term results. The role of other medica-tions for heart failure in the prehospital setting is less clear.Early administration of furosemide appears to have verylittle benefit and may result in short-term complications.33

The prehospital use of morphine sulfate for presumedpulmonary edema is associated with an increased rate ofendotracheal intubation, particularly among patients whoturn out to have been misdiagnosed in the field.33,37

There are few data on the prehospital use ofnoninvasive ventilation (NIV). In one non-randomizedstudy, patients presumed to have congestive heart failure(CHF) were given biphasic positive airway pressure (BiPAP)by the medics during transport and compared to matchedcontrols treated without NIV.38 In this trial, 97% of emer-gency medicine technicians who used BiPAP thought itimproved the patients’ dyspnea; however, data analysisshowed no statistical difference between groups in thelength of subsequent hospital stay, intubation, or mortality.

“The heart monitor, the death cricket bleeping.”—Anne Sexton (1928-1974), U.S. poet.

“The Twelve Dancing Princesses.”29

ED Evaluation

Initial ApproachThe approach to the patient with acutely decompensatedheart failure begins with stabilization of respiratory andhemodynamic status. The emergency physician must thenrapidly exclude or treat reversible conditions. Clinicalevaluation and empiric therapy begin simultaneously withsupplemental oxygen, cardiac monitoring, pulse oximetry,and IV access. Patients with clinical signs of exhaustion orcyanosis despite supplemental oxygen require respiratorysupport by either invasive or noninvasive means (which isdescribed later in the text). Those with hypotension,obtundation, cool extremities, or other signs of poorperfusion should be presumed to be in or near cardiogenicshock and managed accordingly (which is also describedlater in the text). Once the initial resuscitation is under way,further efforts should be made to identify the underlyingcause of decompensation.

HistoryMost patients with heart failure complain of dyspnea ortrouble sleeping. It is important to determine the degree ofdyspnea and its precipitants. Does it occur at rest? Does thepatient have paroxysmal nocturnal dyspnea (PND)? Ask thepatient how he or she has been sleeping and on how manypillows. (Spending the night erect on the sofa is a suspiciousfinding except in the most severe addict of CNN.)

The rapidity of symptom onset may suggest anetiology for the decompensation. An abrupt deteriorationraises concern for arrhythmia, acute coronary syndrome, or

Cost-Effective Strategies For Acutely Decompensated Heart Failure1. Don’t admit every patient with heart failure.

Certain patients with heart failure may require only an

ED “tune-up” and discharge. Patients with a past history of

failure who have a reassuring history and physical

examination, normal laboratory values, and an ECG

unchanged from previous tracings may be candidates for

outpatient follow-up (especially if their decompensation

occurred because they ran out of their medicines). ED

observation units for select patients may also be a cost-

effective alternative to traditional admission.202,203

Caveat: Most patients who present with acutely

decompensated heart failure will need hospital

admission—especially those with abnormal vital signs,

chest pain, or acute exacerbations.

2. Consider the use of CPAP.

CPAP may prevent the need for intubation in some patients

with acute heart failure and can decrease the cost and length

of stay in the intensive care unit. Keeping a machine in the ED

and using it frequently can promote early use.

Caveat: Some patients are not good candidates for

noninvasive ventilation—especially those who are agitated

or those who have altered mental status, unstable vital

signs, or evidence of acute MI.

3. Consider the use of furosemide infusions.

While many patients in acute heart failure respond quickly

to nitrates and bolus diuretics, some do not. According to one

study, intravenous infusions of furosemide for class IV heart

failure are a safe, effective, and economic mode of therapy,

especially in the elderly.98 The increased cost of the infusion

would be more than offset by savings accrued by a shorter

hospital stay. Since this trial was small and non-randomized,

further study is needed to ensure the cost-effectiveness of

this intervention.

4. Utilize BNPs when appropriate.

Of all of the tests available to determine the presence of

acute heart failure, BNP may be the single best investigation.

It is very sensitive and specific and can be performed at

the bedside. In the acute setting, elevated BNP levels

correlate with the diagnosis of heart failure.58 ▲


valvular rupture. Prior episodes of a similar nature canprovide important clues.

Associated symptoms are also important. Determinewhether the patient has had any chest pain or other anginalequivalent such as shoulder, neck, arm or epigastricdiscomfort. The combination of syncope and heart failure isworrisome and is associated with high one-year mortalityrate.39 Ask the patient and family about recent weight gain,leg swelling, urinary output, exercise tolerance, fatigue, andcompliance with diet and medications. New prescriptions orchanges in dosage of suspect drugs such as NSAIDs,ophthalmic beta-blockers, herbals, and over-the-counteragents should be sought.

Medication history is also important in determiningtherapy. Specifically ask male patients with congestivefailure if they are currently taking sildenafil (Viagra). Theadministration of nitrates may cause life-threateninghypotension in such individuals.40

Most patients presenting with decompensatedheart failure will have a prior cardiac history. Patientscan generally tell you if they have had “fluid on the lungs”in the past. More sophisticated patients may be ableto provide details of previous echocardiograms orcardiac catheterizations.

“heart, n. Figuratively, this useful organ is said to bethe seat of emotions and sentiments . . . .

It is now known that sentiments and emotionsreside in the stomach, being evolved from food

by chemical action of the gastric fluid.”—Ambrose Bierce (1842-1914) U.S. journalist,

short-story writer; The Devil’s Dictionary, 1911.29

Physical ExaminationThe patient’s degree of distress should be determined earlyin the encounter; severe pulmonary edema can be a“doorway diagnosis.” Confusion, cyanosis, diaphoresis,inability to speak, falling over on the stretcher, and so onshould prompt a call for the airway cart.

Vital signs not only suggest the severity of illness butcan also indicate etiologic factors. Hyperthermia or hypoth-ermia can occur with sepsis or thyroid disease. In theabsence of rate-controlling pharmacologic agents, tachycar-dia is nearly universal in decompensated heart failure.Bradycardia should raise concern for high-degree AV block,hyperkalemia, digoxin (or other drug) toxicity, or severehypoxia. Hypertension is common in both systolic anddiastolic failure. While hypotension can be baseline forpatients with end-stage cardiomyopathy, in the symptom-atic patient it should raise concern for sepsis, massivepulmonary embolism, or cardiogenic shock. The propor-tional pulse pressure (PPP)—i.e., pulse pressure (systolicminus diastolic pressure) divided by systolic blood pres-sure—provides an approximation of left ventricularfunction, a PPP of less than 25% correlating with a cardiacindex less than 2.2 L/min/m2.19,41

Signs of congestion may be detected by carefulattention to heart and lung sounds, jugular venous disten-

tion (JVD), hepatomegaly, and peripheral edema. Thediagnostic utility of these physical exam findings andrelated maneuvers is well-documented for chronic heartfailure.42,43 Studies performed in the acute setting are scarceand tend to be limited by the lack of “gold-standard”diagnostic criteria. Inter-observer agreement on some ofthese findings is marginal, even in ideal settings.44,45

The pulmonary exam is usually helpful, but it cansometimes be misleading. Rales, a classic finding in heartfailure, may also occur with pneumonia, interstitial lungdisease, or COPD. On the other hand, wheezing, or“cardiac asthma,” is not uncommon in acute heart failure.In acutely dyspneic patients, the sensitivity and specificityof rales for LV dysfunction appears to be quite poor,whereas the constellation of rales, an S3 gallop, and JVD ismore accurate.24

Elevated CVP is present when the top of the external orinternal jugular veins is more than 3 cm vertical distanceabove the sternal angle.46 A positive hepatojugular refluxsign is defined by a rise in the neck veins of greater than 3cm, sustained for more than 15 seconds, that occurs whenthe physician pushes firmly on the patient’s epigastrium.47

In one study, ED patients with acute dyspnea, presence ofhepatojugular reflux had a reported sensitivity and specific-ity of 24% and 96%, respectively, for heart failure.19 AMEDLINE review of the hepatojugular sign found that it ispositive in a variety of conditions, including constrictivepericarditis, right ventricular infarction, restrictive cardi-omyopathy, and left ventricular failure (but only when thepulmonary capillary wedge pressure is greater than 15).47

Heart sounds can be helpful in confirming the diagno-sis of heart failure. In one study of patients with chronicheart failure, an S3 gallop was highly predictive of anabnormal ejection fraction. The absence of an S3, however,was not uncommon in those with a mildly impairedejection fraction.48 A new cardiac murmur in the propercontext must be presumed to signal acute valvular orpapillary muscle dysfunction.

The leg examination is routine in the evaluation ofpatients with suspected heart failure. While pedal edema ishighly specific for increased filling pressures, it has poorsensitivity.43 Unilateral extremity swelling and especially thepresence of a venous cord should raise suspicion for deepvenous thrombosis and possible pulmonary embolism.

Diagnostic Studies

Laboratory TestsThe majority of patients who present with complaintsconsistent with heart failure will need basic laboratorytesting. A complete blood count (CBC) or other measure-ment of hemoglobin is useful for ruling out anemia as acause for decompensation. Some believe that an elevatedwhite blood cell count may suggest an infectious process,especially if bands are present. However, this is not well-studied in the patient who presents with dyspnea. Serumchemistries help assess renal function and overall fluid andelectrolyte balance.


Cardiac MarkersThe question as to which patients with acutely decompen-sated heart failure should get cardiac enzymes is not well-studied. If an acute coronary syndrome is a consideration(e.g., history of chest discomfort or other anginal equivalent,new-onset heart failure, or significant risk factors forcoronary artery disease), serum markers for cardiacischemia/infarction (CK, CK-MB, and troponin) areindicated. Elevated troponins may detect cardiac myolysis(possibly secondary to myocardial wall strain) even in theabsence of coronary artery disease.49 Other studies showthat elevated cardiac troponins may be found in the blood of25%-33% of patients with severe heart failure and help toidentify those with poor short-term prognosis.50

B-Natriuretic PeptideB-type natriuretic peptide (BNP) is an endogenous hormonereleased from the ventricles in response to stretch. BNP is acounter-regulatory hormone, offsetting the effects ofneurohormonal activation by promoting diuresis andvasodilation. Plasma levels of BNP have been shown tocorrelate with degree of left ventricular overload, severity ofclinical heart failure, and both short- and long-termcardiovascular mortality.51-55

Of significance from an ED standpoint, plasma BNPlevels can be used to distinguish between cardiac and non-cardiac causes of dyspnea.56,57 Among patients presentingwith acute dyspnea, a serum BNP level above 94 pg/mLpredicts a diagnosis of heart failure with 91% accuracy.58 In aprospective study of 250 patients with acute dyspneapossibly due to CHF, the mean BNP level was 1076 pg/mLin the CHF group compared with 38 pg/mL in patientswithout CHF. In this study, BNP measurement was moreaccurate than any other single variable, including history,physical, chest x-ray, or ECG.58 Using standard clinicalcriteria, the treating physicians misdiagnosed heart failurein 15 patients subsequently found to have other conditionsand failed to recognize it in 15 additional patients. BNPwould have accurately classified 29 of these 30 patientsusing an 80 pg/mL cut-off.59

For patients with known heart failure, BNP levelsat any given point in time can be compared with baselinemeasurements to form an independent assessmentof clinical severity and may be useful for tailoringspecific therapies.60,61,164

Other TestsArterial blood gases should not be routine in those withacutely decompensated heart failure. They may be useful ifthere is a concern for hypoxia and pulse oximetry is notavailable or if the physician suspects hypercapnia. Patientson digoxin should have serum levels checked.

“But the heart refuses to be imprisoned;in its first and narrowest pulses it already tends outward

with a vast force and to immense and innumerable expansions.”—Ralph Waldo Emerson (1803–1882), U.S. essayist, poet,

philosopher. “Circles,” in Essays, First Series (1841, repr. 1847).29

ElectrocardiogramWhile the ECG is admittedly a relatively insensitivetool, it remains useful for detecting ischemia, arrhythmias,or electrolyte disturbances. Given the high proportionof heart failure exacerbations precipitated by ischemicevents, it is difficult to justify not obtaining an ECG on allsuch patients.15

The ECG is likely to be abnormal in patients with heartfailure. In one study using a clinic population, left ventricu-lar hypertrophy on resting ECG was noted in 42% andelectrocardiographic evidence of cardiac ischemia or a priorMI was present in approximately 70%.62 Comparison withprior ECGs may be critical, especially with patients whohave subtle changes or “baseline abnormal” tracings.

Patients with ECG evidence of acute ischemia orinfarction should be considered for emergent coronaryreperfusion therapy. Importantly, a completely normalECG is strong evidence against the presence of left ventriculardysfunction and should therefore prompt consideration ofalternative diagnoses.24,63

Chest X-rayCombined with a clinical assessment, chest radiography hasbeen reported to be 92% sensitive and 91% specific fordetecting systolic dysfunction.24 The chest film may also beuseful in identifying alternative or contributing causes ofthe patient’s symptomatology.

Findings on chest radiograph can include cardiome-galy, vascular redistribution (e.g., cephalization, fullness ofhilar vessels), interstitial or pulmonary edema, and pleuraleffusions. Pleural effusions in heart failure tend to bebilateral or localized to the right side.64

There are several pitfalls that await the unwaryphysician who uses the chest film to diagnose acute heartfailure. Most importantly, heart size may be normal in acutefailure, especially if the failure originates from acute diastolicdysfunction.43 It is also important to recognize that radio-graphic findings can lag several hours behind clinical signsand symptoms.64 COPD patients may have minimalradiographic evidence of concurrent heart failure, andpatients with prior lung injury may develop focal infiltratesmimicking pneumonia.

Cardiac EchocardiographyFormal echocardiography is invaluable for assessing thestatus of left ventricular function, distinguishing betweensystolic and diastolic failure, and identifying regional wallmotion abnormalities. Echocardiography can also assist indiagnosing or excluding potentially reversible etiologies ofan acute decompensation, such as pericardial tamponade,massive pulmonary embolus, ruptured chordae tendineae,or ruptured ventricular septum.

Whether or not echocardiography is indicated in allinstances of decompensated heart failure remains open todebate.24,64 ACC/AHA guidelines recommend transthoracicechocardiography as soon as possible after initial stabiliza-tion for any patient who presents with acute pulmonaryedema, unless there are obvious precipitating factors and


the patient’s cardiac status has been adequately evaluatedpreviously.16 With the availability of on-call sonographersand timely interpretation via telemedicine,echocardiography can be made operational around theclock.65 Guidelines for establishing an effective system foremergency echocardiography have recently been pub-lished.66 Experience with emergency physicians performingbedside echocardiography has generally been limited toruling out pericardial effusion/tamponade.67-69

Pulmonary Artery CatheterizationMost patients with decompensated heart failure can beevaluated and stabilized in the ED without the introductionof a pulmonary artery (PA) catheter. The literature on therisks and benefits of PA catheterization (also called Swan-Ganz catheterization) in critical illness continues to evolve,but in the case of patients with decompensated heart failure,little is known. ACC/AHA guidelines recommend place-ment of a PA catheter in the setting of acutely decompen-sated heart failure if improvement is not proceeding asexpected, if high-dose nitrates are required for clinicalstabilization, or if inotropic support is needed to augmentsystemic perfusion.16 However, these guidelines were firstissued in 1995, before the publication of more recent dataregarding the dangers of PA catheterization in the criticallyill.70,71 When it is believed necessary, invasive hemodynamicmonitoring can generally be initiated in the CCU.

“I am dying from the treatment of too many physicians.”—Alexander the Great

Treatment

The most important initial interventions will involvemanagement of the airway. Patients with inadequaterespirations will most likely need emergent intubation. Ingeneral, airway management should be accomplished withrapid sequence intubation (RSI). This involves using aninduction agent in combination with a short-acting paralyticsuch as succinylcholine so as to maximize the rate of successon the initial attempt.72 Prolonged episodes of hypoxia orhypotension during intubation risk further cardiac decom-pensation and cardiopulmonary arrest. In one study, allinduction agents used (thiopental, fentanyl, andmidazolam) were associated with a significant risk ofhypotension for patients with pulmonary edema. However,the authors admit that the small numbers of patients withpulmonary edema in this study preclude a valid post hoccomparison.73 On the other hand, induction with etomidateappears to be safe and effective for a range of patientsundergoing RSI, including those with underlying heartdisease.74 Once mechanical ventilation is instituted forcardiogenic pulmonary edema, it is not certain whetherpositive end-expiratory pressure (PEEP) confers anyadditional hemodynamic benefit.75-77

For patients in respiratory distress, application of high-flow oxygen appears beneficial. Although there have beenreports that excessive oxygen can adversely affect leftventricular function, hypoxia is by far the greater concern inthe acute setting.31 Sitting the patient bolt upright may

improve respiratory dynamics. Studies in patients withchronic heart failure show a large rise in airflow resistanceafter lying supine for five minutes, a condition that isreversed by sitting erect.78 Early application of monitorssuch as pulse oximetry, noninvasive blood pressure, andcontinuous cardiac monitoring may provide early warningsof decompensation. While not all patients in acutelydecompensated heart failure require a Foley catheter,monitoring of urinary output with a urinometer can behelpful in those with severe symptoms.

Once immediate threats to airway and breathing areaddressed, the physician must deal with blood pressureemergencies. While hypertensive emergencies resulting inpulmonary edema are life-threatening, they are in generalmore easily amenable to pharmacologic therapy thanhypotensive emergencies associated with acute heart failure.In most cases of shock, fluid challenge is routine andgenerally not harmful, yet in the case of cardiogenic shockthe literature is mute.

Pharmacologic TherapyThe twin objectives of pharmacologic therapy for acutelydecompensated heart failure are relief of pulmonarycongestion and improvement in systemic tissue perfusion.An ideal drug (or drug combination) would reduce preload,enhance left ventricular function, and at the same timemaintain or improve myocardial oxygen balance. While thebasic approach to treating acutely decompensated heartfailure has not changed over the past two decades, there hasbeen increasing emphasis on afterload reduction and othermeans of counteracting the adverse cycle of neurohormonalactivation. (See Table 5 on page 9; see also “ClinicalPathway: Emergency Department Therapy For AcutelyDecompensated Heart Failure” on page 14.)

NitratesNitrates are recommended as first-line therapy for acutelydecompensated heart failure of both ischemic and non-ischemic origin.16 The beneficial hemodynamic effects ofnitrates in the setting of heart failure have long beenappreciated.80,81 At low doses, nitroglycerin inducesvenodilation; at high doses, nitroglycerin causesarteriodilation, including dilation of the coronary arteries.82

Significantly, in patients with severe underlying leftventricular dysfunction, afterload reduction appears topredominate over preload reduction, even at moderatedoses of nitroglycerin.83

A number of studies have compared the hemodynamiceffects of nitrates and diuretics in acutely decompensatedheart failure. In contrast to furosemide, nitrates reduce bothpreload and afterload, and maintain or improve cardiacoutput.84-86 In one head-to-head comparison, a regimen ofhigh-dose nitrates and low-dose diuretics provided moreconsistent clinical improvement than a regimen of high-dosediuretics and low-dose nitrates and was associated withlower rates of mechanical ventilation and MI.87 Becausemany of the patients in this study had underlying coronaryartery disease, it is likely that the anti-ischemic effects ofnitrates played a role.


No other group of agents improves the symptoms ofcongestion as rapidly as nitrates. Treatment with sublingualnitroglycerin (tablets or spray) results in noticeable hemody-namic and clinical improvement within five minutes.88-90

Single doses of 0.4 mg can be given repeatedly every 5-10minutes provided the patient has stable blood pressures. Inthe hospital setting, continuous IV administration ofnitroglycerin is generally more convenient and appropriatefor the more severely ill patient and allows for titration tospecific clinical or hemodynamic end-points. Nitroglycerincan be started at 0.3-0.5 mcg/kg/min so long as the bloodpressure is above 95-100 mmHg.16 Alternative regimens andformulations for administering IV nitrates have beendescribed, but they offer no clear advantages.80,91,92

Transdermal nitroglycerin has comparable hemodynamiceffects to IV nitroglycerin but is less amenable torapid titration and may be less effective in patientswith poor skin perfusion.93

Hypotension with standard nitrate therapy is generallymild and transient. Severe or persistent hypotension shouldraise suspicion for hypovolemia, stenotic valvular disease,cardiac tamponade, right ventricular infarction, or recentuse of sildenafil (Viagra). If these conditions are known orsuspected, nitrates should be avoided or used with extremecaution. Nitrate therapy may not be particularly effective inpatients with massive peripheral edema.94 In such cases,aggressive diuretic therapy is more likely to be of benefit.

Sodium nitroprusside is recommended for patientswith marked systemic hypertension, severe mitral or aorticvalvular regurgitation, or pulmonary edema not responsive

to standard nitrate therapy.16 Nitroprusside directly dilatesresistance vessels, rapidly reducing blood pressure andafterload.80 Typically, nitroprusside is started at a dose of 0.1mcg/kg/min and advanced as needed to improve clinicaland hemodynamic status. Use a systolic pressure of 85-90mmHg as a lower limit provided that adequate systemicperfusion is maintained. In patients with renal failure, long-term use of nitroprusside carries the potential for cyanidetoxicity, as metabolites accumulate. However, this isextremely unlikely during the course of emergency therapy.Nitroprusside has been safely used in the ED treatment ofdialysis patients who presented in acute heart failure.95

DiureticsDiuretics represent the mainstay of therapy for patients withvolume overload. On the other hand, it is important torecognize that patients who present with acutely decompensatedheart failure are not necessarily volume overloaded. Patients withacute diastolic dysfunction, for example, may benefit morefrom redistribution of circulating volume (using nitrates)rather than from diuresis. The indiscriminate use ofdiuretics carries the risk of overdiuresis, particularly amongelderly patients.

Evidence from a large number of in vitro and in vivoexperiments suggest that direct vascular actions alsocontribute to the clinical effects of furosemide.104-107 Theseactions are not necessarily altogether advantageous, in thattheir net effect tends to promote further activation of thesympathetic and renin-angiotensin systems.108,109 Studiescomparing the acute effects of diuretics and nitrates have

Table 5. Medications For Acutely Decompensated Heart Failure.

OxygenAction: Improvement in systemic and myocardial

oxygen balanceIndications: Hypoxia and/or dyspneaCautions/Adverse Effects: Respiratory depression (COPD)Dosing: Titrate to pulse oximetry

MorphineAction: Relief of anxiety; preload reductionIndications: Pulmonary edemaCautions/Adverse Effects: Respiratory depression;

hypotensionDosing: 2-4 mg IV boluses

FurosemideAction: Preload reductionIndications: Volume overloadCautions/Adverse Effects: Hypotension; pre-renal azotemiaDosing: Start 20-40 mg (or twice daily oral dose as IV bolus )

NitroglycerinAction: Preload and afterload reduction; anti-ischemicIndications: Pulmonary edema; myocardial ischemiaCautions/Adverse Effects: Hypotension; toleranceDosing: Start 0.3–0.5 mcg/kg/min IV and titrate upward

NitroprussideAction: Afterload reduction

Indications: Severe hypertension; refractorypulmonary edema

Cautions/Adverse Effects: Hypotension; myocardialischemia; cyanide toxicity

Dosing: Start 0.1-0.2 mcg/kg/min IV and titrateupward

EnalaprilatAction: Afterload reductionIndications: Pulmonary edema; hypertensionCautions/Adverse Effects: Hypotension; hyperkalemiaDosing: 1.25 mg IV

DobutamineAction: Positive inotropy; afterload reductionIndications: Low-output heart failure; refractory

pulmonary edemaCautions/Adverse Effects: Tachycardia; arrhythmia;

hypotension; bronchoconstrictionDosing: Start 2.5 mcg/kg/min IV and titrate upward

MilrinoneAction: Positive inotropy; afterload reductionIndications: Low-output heart failure; refractory

pulmonary edemaCautions/Adverse Effects: Arrhythmia; hypotensionDosing: Bolus 50 mcg/kg over 10 min, then start

0.375 mcg/kg/min IV and titrate upward


emphasized the more favorable overall hemodynamiceffects of the latter group (as described earlier).

Depending on the patient’s clinical condition,state of hydration, and previous use of diuretics, aninitial IV dose of 20-200 mg of furosemide can be adminis-tered. For patients on chronic diuretic therapy, a commonstrategy is to begin with the usual daily dose (typically40-80 mg) given as an IV bolus, and to double the doseif there is inadequate diuresis. In cases of volume overloadthat fail to respond to standard therapy, substitute amore potent loop diuretic such as torsemide (Demadex)10-20 mg IV or bumetanide (Bumex) 1-4 mg IV. Combiningfurosemide with a thiazide agent such as metolazone (5-20mg PO) or chlorothiazide (Diuril 500-1000 mg IV) mayimprove diuresis.96,97

If the patient does not respond to an initial dose or twoof diuretics, another alternative is to administer a high-dose,continuous furosemide infusion at 20-40 mg/hr titrated to aurine output of 100 mL/hr. This will maximize diuresiswhile minimizing the toxicity of comparable bolus furo-semide therapy.98 Other studies support the superiority ofcontinuous furosemide therapy over bolus injection,99,100

with some patients receiving up to 2 grams (yes, 2 grams) offurosemide per day.101 (For a more detailed discussion of thistopic and further references, see the Cochrane Database ofSystematic Reviews.102)

In patients with severe chronic heart failure, regular use

of spironolactone substantially reduces the risk of bothmorbidity and death.110 However, there is no evidencesupporting its use in the ED during an acute episode ofdecompensated failure.

ACE InhibitorsAngiotensin-converting enzyme (ACE) inhibitors representa logical extension of vasodilator therapy. The beneficialhemodynamic effects of ACE inhibitors in acute heart failurehave been appreciated for two decades.111 Acutely, ACEinhibitors reduce both preload and afterload, improve renalhemodynamics, impair sodium retention, attenuatesympathetic stimulation, and maintain or enhance leftventricular function.112-114 In the setting of acute heart failure,drug regimens that include an ACE inhibitor appear tohave hemodynamic advantages over those based onother vasodilators.115-117

For acutely decompensated heart failure, ACE inhibi-tors can be administered intravenously (e.g., enalaprilat[Vasotec IV]), orally (e.g., captopril), or sublingually (e.g.,emptied captopril capsules contents). Depending on thedrug, dose, and route of administration, hemodynamiceffects may be seen within 10-60 minutes.112,113,115 Safe dosingregimens of enalaprilat include 0.004 mg/kg as an IV bolus,or 1.25 mg by infusion over five minutes. The suggestedone-time dose of oral or sublingual captopril is 12.5-25.0 mg.The safety of administering an ACE inhibitor in the setting

Ten Excuses That Don’t Work In Court1. “She was just weak and dizzy. How was I supposed to

know she had heart failure?”

You found out when she went into acute pulmonary edema

after the aggressive fluid bolus! Nonspecific symptoms

such as weakness, lethargy, fatigue, anorexia, or

lightheadedness may be a manifestation of decreased

cardiac output, especially in the older patient. Geriatric

patients can be particularly difficult to evaluate because

they often lack typical signs and symptoms of heart failure.

2. “She was only 35—she couldn’t have had heart failure!”

You can’t diagnose postpartum cardiomyopathy unless

you consider it. Myocarditis, cocaine or alcohol abuse,

and cardiotoxic chemotherapies are important causes of

heart failure in younger patients. While advanced age is a

major risk factor for heart failure, young age should never

exclude it.

3. “He seemed to be wheezing, so I treated him for COPD!”

Unfortunately, his condition continued to deteriorate and

you only learned about his history of heart failure after he

was intubated. Distinguishing between cardiac and

pulmonary causes of dyspnea remains a fundamental

clinical challenge. A careful diagnostic work-up can yield

important clues. Consider the use of BNP if the diagnosis is

not clear.

4. “I just assumed he hadn’t been taking his medications.”

Medication noncompliance and dietary indiscretion

commonly precipitate decompensated heart failure, but

don’t assume this is the case until other serious causes have

been considered. Acute decompensation may be brought

on by a variety of cardiac and non-cardiac conditions,

including ischemia/infarction, arrhythmias, valvular/septal

rupture, sepsis, anemia, and thyrotoxicosis.

5. “He was wide awake and looked extremely anxious. I

thought he could tolerate the 10 mg bolus of morphine!”

This patient stopped breathing and had to be precipitously

intubated. Injudicious use of opiates can result in excessive

sedation and loss of respiratory drive. Although useful in

small doses for relieving anxiety, opiates provide little

hemodynamic benefit in patients with pulmonary edema.

6. “She was clearly ‘wet’ and needed to be aggressively

diuresed. Is it my fault her creatinine doubled by the

next day?”

Continued on page 11


of acutely decompensated heart failure is of concern to someclinicians who fear potentially deleterious effects on bloodpressure, renal function, and electrolyte balance. However,clinical trials have consistently demonstrated the safety ofadministering ACE inhibitors to patients with acutelydecompensated heart failure.114,118

Few studies of ACE inhibitors for acutely decompen-sated heart failure have been performed in the ED setting.Small studies have demonstrated that sublingual captoprilis safe and effective for ED patients with pulmonaryedema.95,119 In one retrospective analysis, the use of sublin-gual captopril in the ED was associated with lower rates ofmechanical ventilation and CCU admission.120

ACE inhibitors are contraindicated in the context ofpregnancy, hyperkalemia, or a history of ACE-inhibitor-induced angioedema. For patients with evidence ofpoor systemic perfusion, ACE inhibitors should be usedcautiously, because additional vasodilation may notbe tolerated. Unlike nitrates, ACE inhibitors have a rela-tively prolonged duration of action, making dosage lesseasily titratable.

InotropesWhile the role of long-term inotropic therapy for chronicheart failure remains controversial, short-term therapy inacutely decompensated failure appears to benefit selectpatients. Classically, inotropic agents have been reserved for

the treatment of cardiogenic shock. However, short-terminotropic support may also be beneficial for patients whofail to respond to (or who are not candidates for) conven-tional therapy with diuretics and vasodilators.16 Whileshort-term inotropic therapy clearly improves hemody-namic performance, data on clinical outcomes are limited.

In the absence of frank cardiogenic shock, inotropicsupport is typically initiated using an agent that bothincreases myocardial contractility and reduces afterload.This class of “vasodilator inotropes” includes beta-agonistssuch as dobutamine as well as the phosphodiesteraseinhibitors amrinone, milrinone, and enoximone. (See Table 5on page 9.) Small trials with each of these agents havedemonstrated short-term hemodynamic improvement inpatients with acutely decompensated heart failure, mostcommonly in the setting of MI.123-127 The addition of low-dose nitrate therapy to an inotropic regimen may conferadditional hemodynamic benefits.128,129 In one head-to-headcomparison in patients who sustained heart failure follow-ing an acute MI, milrinone (50 mcg/kg bolus over 10minutes, infusion at 0.25-0.75 mcg/kg/min) appeared toconfer more consistent short-term hemodynamic improve-ment than dobutamine (infusion at 2.5-15.0 mcg/kg/min).130

Other evidence suggests some advantage in milrinone overdobutamine in patients with severe heart failure even in theabsence of acute MI.131 As we see more heart failure patientsmaintained on chronic beta-blocker therapy, the theoretical

Ten Excuses That Don’t Work In Court (continued)

Maybe. This elderly woman with acute diastolic dysfunction

was not suffering from volume overload. Her pulmonary

congestion may have responded better to vasodilator

therapy than to aggressive diuresis that ended up

impairing her renal function and prolonging her

hospital stay.

7. “I always thought sublingual nitroglycerines were

harmless. I didn’t expect his systolic BP to drop to

single digits!”

Nitrates are fast, effective, and relatively safe, but patients

with preload-dependent conditions (e.g., valvular stenosis)

do not tolerate them well. Nor do patients taking Viagra!

8. ”He was in severe respiratory distress, so he had to be

intubated. Who would have thought he would spend a

week in the CCU!”

Maybe if you had considered CPAP, the patient could have

avoided the ventilator-associated pneumonia and

prolonged CCU stay. For patients with severe cardiogenic

pulmonary edema, CPAP can reduce the need for

endotracheal intubation and decrease length of ICU stay.

9. “He was in rapid atrial fibrillation, and I figured rate-

control would improve his cardiac function.”

Unfortunately, you failed to consider the negative inotropic

effects of verapamil, and the patient’s heart failure further

decompensated. When a patient presents with

decompensated heart failure in the context of rapid atrial

fibrillation, it is important to address the clinical situation

as a whole, which means treating for both conditions

simultaneously and recognizing that the treatment of

the one may impact upon the other. If the emergency

physician believes that new-onset atrial fibrillation has

precipitated acute pulmonary edema, emergent

cardioversion is indicated.

10. “She felt a little better after the Lasix, so we sent

her home 10 minutes later. Her short length of stay

was impressive!”

But when she came back the next day in florid pulmonary

edema, she ended up in the CCU. There is growing evidence

that premature release of patients with inadequately

treated heart failure is associated with increased short-term

morbidity and mortality. While published guidelines can

help guide the decision to admit, it is important to

recognize that even “low-risk” patients have considerable

potential for morbidity. ▲


advantages to phosphodiesterase inhibitors over beta-agonists increase.132

It is important to understand the expected hemody-namic effects of inotropic agents and set clear goals fortherapy. Most inotropic agents have multiple pharmacologicactions, some of which may be deleterious. Undesirablechronotropic effects, arrhythmogenesis, or ischemiaresulting from increased myocardial oxygen consumptionmay curtail the use of any particular drug.

Digoxin has a very limited role in the ED managementof heart failure. The inotropic effects of digoxin are modest,unpredictable, and delayed for at least 90 minutes after IVloading.123 For patients with acutely decompensated heartfailure, the only reasonable use for digoxin is to help controlthe ventricular response to atrial fibrillation (as describedlater in the text).

MorphineMorphine is one of the oldest drugs still in use for thetreatment of acute heart failure and remains an importantadjunct for treating the anxiety and discomfort associatedwith pulmonary edema. With high doses of morphine,direct vasodilation may result from histamine release, butthe predominant hemodynamic effects of morphine appearto be mediated through the central nervous system.133

Morphine can be administered safely to most patients.However, because of its sedative properties and potential todepress respirations, exercise caution when administeringmorphine in the setting of chronic pulmonary insufficiencyor suspected acidosis. One retrospective study found thatED administration of morphine to patients with pulmonaryedema was associated with an increased rate of endotra-cheal intubation and CCU admission.120

Respiratory TherapyThe majority of patients with respiratory distress respond tosupplemental oxygen and standard pharmacologic therapy,but patients with persistent hypoxemia or progressivefatigue will require at least temporary respiratory support.(See also the July 2001 issue of Emergency Medicine Practice,“Noninvasive Airway Management Techniques: How AndWhen To Use Them.”)

Mask-applied continuous positive airway pressure(CPAP) of 5-10cm H2O has been shown in several random-ized, controlled clinical trials to reduce the need for endotra-cheal intubation in patients with severe cardiogenicpulmonary edema.134-136 Pooled data also suggest that theuse of CPAP in this setting may be associated with de-creased mortality.137 CPAP improves lung mechanics byrecruiting atelectatic alveoli, improving pulmonary compli-ance, and reducing the work of breathing.138 At the sametime, particularly in patients with CHF, CPAP improveshemodynamics by reducing preload and afterload, therebyenhancing left ventricular performance.139-142

BiPAP—or noninvasive positive pressure ventilation(NPPV)—provides the physiological advantages of CPAPduring expiration but provides additional assistance withthe inspiratory work of breathing. Evidence from several

case series and a recent randomized trial supports the use ofthis therapy in patients with acute cardiogenic pulmonaryedema.143-147 A small, randomized trial comparing BiPAPwith CPAP demonstrated a more rapid clinical improve-ment with BiPAP but no difference in the rates of intuba-tion.148 Of concern in this trial was an unexpectedly high rateof acute MI associated with the use of BiPAP, whichprompted premature termination of the study. One otherclinical trial involving BiPAP was also terminated earlybecause of similar safety concerns.149 At present, it seemsprudent to employ CPAP rather than BiPAP for patientswith cardiogenic pulmonary edema and hypoxemicrespiratory failure.150

The success of noninvasive respiratory supportdepends on appropriate patient selection. For patients withcompromised upper airway function or significantly alteredlevel of consciousness, intubation and mechanical ventila-tion remain the definitive therapy. Patients with a history ofcardiac arrest, unstable cardiac rhythms, or cardiogenicshock are generally not felt to be candidates for noninvasiveapproaches. Likewise, in the setting of severe myocardialischemia or infarction, full ventilatory support may bepreferable in order to decrease the myocardial oxygendemand associated with respiratory effort.

Although the decision to initiate noninvasive respira-tory support is dependent on a variety of factors, thepresumption is that the earlier therapy is instituted, thegreater the likelihood of averting intubation. Recent studiessuggest that the use of noninvasive ventilatory support inthe prehospital setting is feasible and potentially beneficialfor patients with presumed cardiogenic pulmonaryedema.38,151 If there is progressive respiratory failure in spiteof noninvasive support, the patient requires intubation andmechanical ventilation.

Special Circumstances

“But his flawed heart / (Alack, too weak the conflict to support!) /‘Twixt two extremes of passion, joy and grief, / Burst smilingly.”

—William Shakespeare (1564–1616),in King Lear, act 5, sc. 3, l. 197-200.

Cardiogenic ShockHypotension in the setting of decompensated heart failure ispresumed to be due to cardiogenic shock and requiresaggressive management. Regardless of blood pressure,patients who present with evidence of inadequate tissueperfusion (i.e., cool skin, altered mental status) should beapproached in the same manner. Mortality rates for patientswith frank cardiogenic shock remain alarmingly high,ranging from 50% to 80%.152 Although there is a lack of datafrom controlled trials regarding the optimal management ofthese patients, consensus guidelines offer some direction.16

Cardiogenic shock is most often seen in the setting ofacute ST-segment elevation MI, but it occurs in other acutecoronary syndromes as well.153 In the context of acute MI,emergent cardiac catheterization and revascularization improvesoutcome and should be strongly considered.154 In the absence of

Continued on page 19


The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon apatient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copyingprivileges for educational distribution within your facility or program. Commercial distribution to promote anyproduct or service is strictly prohibited.

Clinical Pathway: Prehospital TherapyFor Acutely Decompensated Heart Failure

Impending respiratory failure?

• Upright sitting position (Class indeterminate)• Oxygen therapy (Class I)• Cardiac monitor (12-lead ECG if available; Class

indeterminate)• IV access (Class I)

• Endotracheal intubation (Class I) or CPAP if availableand no contraindications (see text) (Class II)

• Alert ED regarding patient status

Expedite transport to the ED

• SL TNG/Nitro-Spray (Class II)• IV furosemide* (Class III)• IV morphine* (Class III)

* These drugs can cause complica-tions if patient is misdiagnosed aspulmonary edema in the field

• ASA (Class I)• SL TNG/Nitro-Spray (Class II)• IV morphine (Class II)

• ACLS interventions (Class I-III;use caution with calcium-channel blockers and beta-blockers)

→ →

Pulmonary edema? Chest pain? Arrhythmia?

→→ →

→→

→

→

→→





Clinical Pathway: Emergency Department TherapyFor Acutely Decompensated Heart Failure

• Upright sitting position (Class indeterminate)• Oxygen therapy (Class I)• Chest x-ray (Class I)• Cardiac monitor and 12-lead ECG (Class I)• Pulse oximetry (Class I-II)• IV access (Class I)• Foley catheter if significant distress (Class indeterminate)

→

→

• Acute MI, persistent cardiacischemia?

Yes→ • ASA (Class I)• percutaneous transluminal coronary angioplasty (PTCA)

(Class I)• Thrombolytics (Class I-II for ST-elevation MI)

→No

→• Unstable tachycardia?

Yes→

Go to top of next page

• Determine if patient is a candidate for cardioversion(ventricular tachycardia or acute-onset atrial fibrilla-tion, atrial flutter) (Class II)

• Antiarrhythmic therapy* (Class II)

*Special caution needed with beta-blockers and calcium-channel blockers due to negative inotropy

No

→

• Cardiogenic shock?

No

→

• Pressors/inotropes (Class II)• Inra-aortic balloon counterpulsation (IABC) if potentially

reversible etiology (Class II)• Cardiology consult (Class indeterminate)

Yes→

→

• Compromised upper airway function?• Altered level of consciousness?• Hemodynamic instability/cardiogenic shock?• Myocardial infarction or severe ischemia?

Consider CPAP(Class II)

Endotrachealintubation (Class I)

• Persistent respiratory distress?Yes→

→ →

Yes No

No

→





Clinical Pathway: Emergency Department TherapyFor Acutely Decompensated Heart Failure (continued)

If inadequate clinical improvement

Nitrates*• Sublingual while starting IV or if moderate symptoms (Class II)• Transdermal if good skin perfusion no significant diaphoresis (Class III)• Intravenous nitroglycerin if severe distress or significant hypertension (Class I-II): start at 0.3-0.5 mcg/kg/min and titrate to

blood pressure and symptoms

*Do not use if patient taking sildenafil (Viagra)

→

Add diuretics*• Furosemide twice daily dose intravenously or start with 40-80 mg IV (Class II)• If inadequate urinary output, consider one or more of the following:

• Double furosemide dose (Class II)• Add different loop diuretic (torsemide [Demadex] or bumetanide [Bumex]) (Class III)• Add thiazide diuretic (Chlorothiazide [Diuril] or other) (Class II)• Begin furosemide infusion: start at 20-40 mg/h, titrate to achieve urine output of 100 cc/h (Class II)

*Avoid diuretics in case of acute diastolic dysfunction (flash pulmonary edema with presumed ischemia) and in case of hypotension→

→

Add ACE inhibitors*• Enalapril 1.25 mg IV given over 5 minutes (Class II-III)• Captopril 12.5-25.0 mg PO or SL (Class II-III)

*Avoid in hypotension, pregnancy, hyperkalemia, or a history of ACE-inhibitor-induced angioedema

Add inotropes• Milrinone (50-mcg/kg bolus over 10 minutes, infusion at 0.25-0.75 mcg/kg/min) (Class I-II)• Dobutamine (infusion at 2.5-15.0 mcg/kg/min) (Class I-II) →

Go to top of next page

Consider morphine sulfate (2-3 mg boluses) for anxiety as needed (Class II-III)


→→


→→


• New murmur?• Unexplained etiology for pulmonary edema?• Clinical exam suspicious for tamponade?• Shock?

Pericardial tamponade? Valve/septal rupture?




Clinical Pathway: Emergency Department TherapyFor Acutely Decompensated Heart Failure (continued)

→

Diagnostic studies• Cardiac enzymes: Sudden/rapid onset, anginal pain, ischemic changes on ECG, or significant risk factors for coronary artery

disease (Class II)• B-natriuretic peptide: Possible competing diagnosis or unclear clinical picture (Class II)• Electrolytes (Class II)• CBC or hemoglobin (Class II-III)

Emergent or urgent transthoracic echocardiography depending on clinical stability (Class II)→

Yes

Disposition according to clinical status

→ →

→ →

Pericardiocentesis (Class II) Cardiothoracic consult (Class II)

→ →

→


• Atrial fibrillation/atrial flutter?

• Fluid overload in renal failure?

• Uncontrolled hypertension?

• Infection/sepsis?




Clinical Pathway: Emergency Department TherapyFor Acutely Decompensated Heart Failure—Special Circumstances

Yes→

No

→

• Consider cardioversion for new-onset atrial fibrillation(Class II; Class I if unstable patient with new-onset atrialfibrillation)

• Rate control:• IV/PO diltiazem (Class II)• IV amiodarone (Class II)• IV/PO digoxin (Class II)

Yes→

No

→

• Dialysis (Class I)• IV nitroglycerin (Class II)• IV nitroprusside (Class II)• IV/PO ACE inhibitor (Class II)• IV furosemide (Class II)

Yes→

No

→

• IV nitroglycerin (Class I-II)• IV nitroprusside (Class I-II)• IV/PO ACE inhibitor (Class II)• IV furosemide (Class II)

Yes→• Antibiotics (Class I)• Pressors (Class I-II)• Fluids (Class II)


Tool 1. Sample Discharge Instructions For ED Heart Failure Patients.

You have been evaluated and treated for symptoms of heart failure in the emergency department.Your condition has sufficiently improved or stabilized so that you will be discharged from theemergency department for outpatient follow-up. However, your heart failure may deteriorate onceagain, in which case you should return to the emergency department.

If you experience any of the following, please return to the emergency department immediately:1.Chest pain or discomfort2.Progressive shortness of breath3.Fainting or lightheadedness4.Persistent palpitations or (new) irregular pulse5.Significantly reduced amount of urine6.Persistent cough7.Wheezing8.High fever or shaking chills9.Any new, different, or worsening problem

Follow-up Instructions

• Return to emergency department for re-evaluation in _______ hours/days.• Check in with your doctor (Primary Care Provider or Cardiologist) if not improved in _______ days.• Check in with your doctor (Primary Care Provider or Cardiologist) in _______ days.• You will need to have the following (x-rays/tests) checked in _______ days: ________________• You may need to have an outpatient (stress test/echocardiogram). This (has/has not) been

discussed with your regular doctor.

Medications

Take the following medicines as prescribed:________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

Additional Instructions

1.Avoid salty foods.2.Limit fluid/water intake as instructed (daily fluid restriction: _______ ).3.Keep a daily measurement of your weight in a logbook for your doctor to see.4.Visiting Nurse/Home Health Aide/Social Work/Outpatient Heart Failure Team has been arranged.

They will contact and check on you within _______ days.5.Read through the provided heart failure materials, and contact your regular doctor if you have

any questions.



emergent catheterization, thrombolysis may be useful,especially when given in combination with intra-aorticballoon counterpulsation (IABC).155 Other potentiallyreversible causes of cardiogenic shock, such as acutevalvular dysfunction, septal rupture, and pericardialtamponade, need to be excluded or addressed promptly.Non-cardiac etiologies of shock, such as hypovolemia,sepsis, poisoning, and massive pulmonary embolism, mustalso be entertained.

As mentioned previously, the use of a fluid bolus totreat cardiogenic shock is not well-studied. While conven-tional wisdom holds that hypotension due to a rightventricular infarction generally responds well to fluidinfusion, some data call this notion into question.156,157

Patients who present in shock with a normal bloodpressure or with mild hypotension often respond favorablyto dobutamine (starting at 2-3 mcg/kg/min). Comparedwith dopamine, dobutamine is associated with a lowerincidence of arrhythmias, less peripheral vasoconstriction,and more consistent reduction in left ventricular fillingpressure for a comparable rise in cardiac output.158

Dopamine is required for patients who have severe orpersistent hypotension (systolic blood pressure < 70-80mmHg) in the presence of volume overload or after bolusadministration of saline. At moderate doses (4-5 mcg/kg/min), dopamine improves cardiac output without causingexcessive systemic vasoconstriction. If the patient can bestabilized with dopamine, dobutamine can then be addedand the dose of dopamine reduced, with the goal ofreducing myocardial oxygen demand.

If hypotension or clinical shock persists at dopaminedoses of 15 mcg/kg/min or greater, IABC should beconsidered, presuming the patient has a potentially reversiblecondition. For example, IABC can be an effective temporiz-ing measure in anticipation of coronary revascularization orcardiac valve repair. Likewise, a patient with massive beta-blocker overdose can be maintained on IABC until the drugis metabolized or otherwise removed from the body.159 Thepatients least likely to benefit from the IABC are those withmultiple previous infarctions, massive irreversible myocar-dial necrosis, advanced stages of cardiogenic shock, andelderly patients with peripheral vascular disease (because ofcomplications from insertion of the device). If IABC is notimmediately available, norepinephrine can be added toincrease systolic pressure to acceptable levels (≥ 80 mmHg).Because of the adverse effects on renal and mesentericperfusion, the use of high-dose dopamine or norepinephrineshould be considered only as a temporizing measure until adefinitive therapy can be substituted.

Dialysis PatientsHeart failure is present in about one-third of patients whobegin dialysis and will develop over time in an additional25%.160 Among anuric hemodialysis patients, heart failure isthe most common cause of ED visits.161 In these patients,acutely decompensated failure is most often due to volumeoverload between dialysis treatments. Although hemodialy-

sis is the treatment of choice for these patients, it may not beimmediately available. ED treatment is directed at stabiliz-ing these patients until hemodialysis can be performed.

Because of their direct vascular effects, diuretics maystill have a role in managing anuric patients with volumeoverload.162 Vasodilator therapy with nitrates and ACE inhibitorshas been shown to be particularly effective.95 In any dialysispatient with an unstable cardiac rhythm, hyperkalemia anddigoxin toxicity must be considered.

An older therapy that is sometimes considered whendialysis is unavailable and other interventions fail is theadministration of oral sorbitol (100 mg PO). This interven-tion draws intravascular fluid into the gut, which is thenexcreted in the diarrheal stool.163

Atrial FibrillationAtrial arrhythmias, and atrial fibrillation in particular, arecommonly seen in patients with chronic heart failure. Infact, it is frequently the same underlying condition—e.g.,hypertension, coronary artery disease, or valvular disease—that predisposes the patient to both atrial fibrillation andheart failure. In the context of normal ventricular function,loss of synchronized atrial contractions is of minimalhemodynamic significance. However, in patients who haveabnormal systolic or diastolic function, the loss of “atrialkick” can have profound consequences. Moreover, whenatrial fibrillation is accompanied by a rapid ventricularresponse, the tachycardia itself is problematic because itmeans reduced filling time and increased myocardialoxygen demand.

When assessing the patient with rapid atrial fibrillationand acutely decompensated heart failure, it is often difficultto attribute cause and effect. Was the onset of rapid atrialfibrillation a response to worsening heart failure (e.g., vianeurohormonal activation and/or increased atrial stretch)?Alternatively, did ventricular function deteriorate becauseof the onset of rapid atrial fibrillation? Rather than riskgetting caught up in a “chicken-and-egg” debate, theimportant point is to address the patient’s clinical statusas a whole. Often this means treating for both conditionssimultaneously, recognizing that the treatment of the onemay impact upon the other. For example, use of a beta-blocker or calcium-channel blocker for rate control mayhave negative inotropic effects that worsen existing systolicdysfunction. On the other hand, use of an inotropic agentlike dobutamine to enhance myocardial contractility mayresult in a faster ventricular rate. In general, diltiazemand amiodarone (and, to a lesser extent, digoxin) areconsidered first-line therapies for rate control in patientswith left ventricular dysfunction.166-168 Electrical cardioversionmay be life-saving for the unstable patient who has acute atrialfibrillation. However, maintaining sinus rhythm may not bepossible if the underlying heart failure is not addressed.

Controversies/Cutting Edge

Impedance CardiographyImpedance cardiography (IC) is a noninvasive means of

Continued from page 12


hemodynamic monitoring, capable of providing real-timeestimates of cardiac output and pulmonary capillary wedgepressure by employing principles of thoracic bioimpedance.Over the past three decades, IC has been investigated in avariety of clinical settings and has been found to comparemoderately well with other modalities for assessinghemodynamics (e.g., echocardiography, Swan-Ganzcatheterization).169,170 Because the technique is noninvasive,portable, and capable of providing beat-to-beat information,potential applications in the ED are numerous.171 IC is lessaccurate in patients with underlying heart disease, but serialmeasurements may still provide useful information—forexample, for monitoring response to therapy.170 Also, theremay be a distinct role for IC in helping to differentiatebetween systolic and diastolic dysfunction.171

Beta-blockersLarge randomized, controlled trials have demonstratedclear benefits for long-term beta-blocker therapy inpatients with systolic heart failure.172-174 In contrast,short-term administration of beta-blockers to patientswith severe systolic dysfunction can cause life-threateningclinical deterioration.175 Therefore, beta-blockers are notroutinely recommended for treatment of acutely decompensatedheart failure. In the setting of an acute decompensation,chronic beta-blocker therapy should either be temporarilydiscontinued or administered cautiously at a reduceddose. When decompensated heart failure occurs in thecontext of an acute coronary syndrome, the risk of worsen-ing heart failure must be weighed against the knownbenefits of beta-blockade.176-178

Less is known about the safety and efficacy of beta-blocker therapy for patients with acute diastolic dysfunc-tion. In theory, the value of reducing hypertension andtachycardia would outweigh any concern about negativeinotropy in these patients. Anecdotal experience with beta-blockers—for example, in the management of hypertensivecrises—has been positive. Further studies are needed toclarify the role of beta-blockers in the treatment of acutediastolic dysfunction.

B-Natriuretic PeptideAs a naturally occurring counter-regulatory hormone, BNPalso has therapeutic potential. Like the other natriureticpeptides in its class, BNP exerts favorable hemodynamic,

natriuretic, and neurohormonal effects when administeredin supraphysiologic doses.179-182 Studies show that nesiritide(Natrecor), a recombinant form of BNP, improves short-termhemodynamic function and clinical status in patientshospitalized with decompensated heart failure.183 The FDAhas recently approved this drug for the treatment of heartfailure. Like other vasodilator agents, the major adverseeffect of nesiritide is hypotension.

Whether or not there is a role for nesiritide in the EDremains unclear. A multicenter, randomized clinical trial ofnesiritide in an ED-based heart-failure observation-unitsetting is currently under way (PROACTION).

Calcium SensitizersCalcium sensitizers (levosimendan, pimobendan) are anovel class of agents that modify the configuration oftroponin C to promote myofilament sensitivity to calcium,enhancing contractility without impeding diastolic relax-ation.184 In small studies of patients with severe decompen-sated heart failure, these agents have been shown to be aseffective as dobutamine and milrinone in increasing cardiacoutput and reducing pulmonary capillary wedge pressure,but without increasing myocardial oxygen demand asconventional inotropes do.185,186 Implications for ED utiliza-tion await additional clinical trials.

Disposition

Even in this era of cost containment, the vast majority ofpatients who present with decompensated heart failure areadmitted to the hospital.18 Meanwhile, hospital costs forinpatient care of decompensated heart failure are continuingto rise. In 1996, an average of over $5000 was paid on behalfof Medicare beneficiaries per hospital discharge for heartfailure.2 However, while the realities of modern healthcareeconomics may not favor routine hospitalization, prematurerelease of inadequately treated patients is likely to increaseshort-term morbidity and mortality.187 Alarmingly, a recentoutcome study of 112 patients discharged from the ED witha primary diagnosis of CHF showed that within threemonths of the initial visit, more than 60% experienced arecurrent ED visit, hospitalization, or death.13

In general, clinicians have great difficulty judging theprognosis of patients with exacerbations of heart failure.188

Acutely decompensated heart failure is a dynamic entity,and the ED physician is with the patient for only a shorttime. Some patients are dramatically ill at presentation butrespond rapidly to treatment, while others deteriorate aftera period of relative stability.

Previous studies have found that certain patientcharacteristics predict in-hospital morbidity and mortality.Multivariate analyses have found several independentcorrelates of major complications or death during hospital-ization.6,9,189,190 These include hypotension, tachypnea,jugular venous distention, electrocardiographic abnormali-ties, hyponatremia, and poor initial diuresis.

A number of other characteristics have also beencorrelated with in-hospital mortality.6,8-11,15,189,191-195 (See Table6.) Disturbingly, even patients without any independent risk

Table 6. Correlates Of In-Hospital Mortality.

• Advanced age• New onset of heart failure• Prolonged duration of symptoms• Poor left ventricular (LV) function• Chest pain• Hypotension• Jugular venous distention• Non-sinus rhythm and ECG abnormalities• Elevated creatine kinase levels• Digoxin use• Advanced renal dysfunction• Poor response to initial therapy


factors appear to have substantial rates (6%) of in-hospitalmorbidity and mortality.6

The AHCPR has established criteria for hospitalizationof patients with heart failure.17 (See Table 7.) However, inone study, these criteria failed to identify up to one-third ofthe patients who die within 30 days.18 In this same study, theED physician’s clinical judgment appeared to be a betterpredictor of 30-day mortality. ACC/AHA guidelines statethat in the absence of specific criteria (e.g., recent MI, symptom-atic arrhythmias, marked hypokalemia), patients with “mild-to-moderate symptoms” are generally at low risk and do not requirehospital admission. Using ACC/AHA definitions, over half ofthe patients admitted for heart failure may be “low risk,” yetup to 5% of these “low-risk” admissions are associated withan adverse cardiovascular event.196 Thus, while publishedcriteria and guidelines can help with triage, the significantrate of morbidity even among “low-risk” patients mandatesthat clinical judgment be incorporated into the decision-making process.

ACC/AHA guidelines explicitly allow for an observa-tion period prior to determining a patient’s disposition.16

During this period of time, patients can be monitored fortheir response to therapy and for the development of anypotentially serious adverse events. Theoretically, an ED-based observation unit or other subacute care setting canaccomplish this at substantial cost savings. Observationunits have been advanced as a safe and effective means ofreducing hospital admissions in general and heart failureadmissions in particular.197,198 Appropriate patient selectionis critical for the functioning of such units. (See Table 8.)

For patients who are ultimately discharged home,consultation with the patient’s primary care physician and/or cardiologist is imperative. Patients and their familiesneed to understand that there is a substantial chance ofoutpatient failure necessitating a repeat ED visit or hospital-ization within the next 30 days.13 Depending on whatprecipitated the decompensation, the patient’s outpatientdrug regimen may require some adjustment. Intensiveoutpatient follow-up has been shown to be successful inpreventing repeat visits to the ED.199,200 Referral to anoutpatient heart failure program where available can reducethe frequency of ED visits and hospitalizations.201 Sampledischarge instructions are shown on page 18. ▲

References

Evidence-based medicine requires a critical appraisal of theliterature based upon study methodology and number ofsubjects. Not all references are equally robust. The findingsof a large, prospective, randomized, and blinded trialshould carry more weight than a case report.

To help the reader judge the strength of each reference,pertinent information about the study, such as the type ofstudy and the number of patients in the study, will beincluded in bold type following the reference, whereavailable. In addition, the most informative references citedin the paper, as determined by the authors, will be noted byan asterisk (*) next to the number of the reference.1.* Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart

J 1991;121:951-7. (Review)2. American Heart Association. 2000 Heart and Stroke Statistical

Update. Washington, DC: American Heart Association; 2000.(Review)

3. McCaig LF, Burt CW. National Hospital Ambulatory Medical CareSurvey (NHAMCS): 1999 Emergency Department Summary. AdvData 2001;320:1-36. (Epidemiologic survey)

4. Allegra JR. Monthly, weekly, and daily patterns in the incidence ofcongestive heart failure. Acad Emerg Med 2001;8:682-685.(Retrospective chart review; 26,224 patients)

5. Daley J, Jencks S, Draper D, et al. Predicting hospital-associatedmortality for Medicare patients. A method for patients withstroke, pneumonia, acute myocardial infarction, and congestiveheart failure. JAMA 1988;260:3617-3624. (Retrospective, cohort;5888 patients)

6.* Chin MH, Goldman L. Correlates of major complications or deathin patients admitted to the hospital with congestive heart failure.Arch Intern Med 1996;156:1814-1820. (Prospective, cohort;435 patients)

7. Jaagosild P, Dawson NV, Thomas C, et al. Outcomes of acuteexacerbation of severe congestive heart failure: quality of life,resource use, and survival. Arch Intern Med 1998;158:1081-1089.(Prospective, cohort, multi-center; 1390 patients)

8. Plotnick GD, Kelemen MH, Garrett RB, et al. Acute cardiogenicpulmonary edema in the elderly: factors predicting in-hospitaland one-year mortality. South Med J 1982;75:565-569. (Prospective,observational; 55 patients)

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10. Le Conte P, Coutant V, Nguyen JM, et al. Prognostic factors inacute cardiogenic pulmonary edema. Am J Emerg Med 1999;17:329-332. (Prospective, cohort; 186 patients)

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12. Barron HV, Every NR, Parsons LS, et al. Investigators in theNational Registry of Myocardial Infarction 2. Am Heart J 2001

Table 7. AHCPR Criteria For Hospital Admission.

• Myocardial ischemia• Pulmonary edema/severe respiratory distress• Hypoxia (oxyhemoglobin saturation < 90%)• Anasarca• Severe complicating medical disease• Symptomatic hypotension or syncope• Heart failure refractory to outpatient management• Inadequate social support for safe outpatient

management

Table 8. Observation Unit Heart Failure Protocol—Exclusion Criteria.

• Alternative diagnosis primarily responsible for acutesymptoms (e.g., chronic obstructive pulmonary disease,pneumonia, arrhythmia)

• Acute myocardial infarction or persistent anginalchest pain

• New persistent oxygen requirement• Requirement for mechanical ventilation (including

noninvasive ventilatory support)• Requirement for vasopressor/inotropic agents to support

hypotension• Requirement for nitroprusside to control hypertension• Requirement for emergent hemodialysis• Severe complicating medical disease• Inadequate social support for expected disposition to

safe outpatient management


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198. Graff LG, Krivenko C, Maag R, et al. Emergency DepartmentEvaluation of Congestive Heart Failure: The Appropriate Evaluation andTreatment of DRG 127. Farmington, Conn: VHA of Southern NewEngland; 1995. (Review)

199. Chapman DB, Torpy J. Development of a heart failure center; amedical center and cardiology practice join forces to improve careand reduce costs. Am J Manag Care 1997;3:431-437.

200. West JA, Miller NH, Parker KM, et al. A comprehensivemanagement system for heart failure improves clinical outcomesand reduces medical resource utilization. Am J Cardiol 1997;79:58-63. (Prospective; 51 patients)

201. Krumholz HM, Baker DW, Ashton CM, et al. Evaluating quality of


care for patients with heart failure. Circulation 2000;101:e122.(Review)

202. Peacock WF 4th, Albert NM. Observation unit management ofheart failure. Emerg Med Clin North Am 2001 Feb;19(1):209-232.(Review, tutorial)

203. Albert NM, Peacock WF: Patient outcome and costs afterimplementation of an acute heart failure management program inan emergency department observation unit. J Internat Soc HeartLung Transplant 1999;18:92.

Physician CME Questions

17. Diastolic failure primarily involves impairment of:a. myocardial contractility.b. ventricular filling.c. atrioventricular conduction.d. systemic vascular resistance.

18. Progressive severe respiratory distress in theprehospital setting should be addressed with:a. prone positioning.b. continuous high-dose furosemide infusion.c. CPAP with ambient air.d. endotracheal intubation.

19. Which of the following tests is unlikely to behelpful in patients presenting with decompensatedheart failure?a. Cardiac enzymesb. BUN/creatininec. Amylased. CBC

20. The most common cause of cardiogenic shock is:a. acute ST-elevation MI.b. ventricular septal rupture.c. pericardial tamponade.d. mitral valve chordae rupture.

21. A patient with new cardiac murmur and acute onsetof heart failure needs to have which of the follow-ing studies performed emergently?a. Gated myocardial scanb. Cardiac MRIc. Blood culturesd. Transthoracic echocardiography

22. What percentage of “low-risk” heart failureadmissions have an adverse cardiovascular eventduring their in-hospital stay?a. 45%b. 33%c. 5%d. < 2%

23. Some patients presenting to the ED with decom-pensated heart failure have sustained an acute MI.a. Trueb. False

24. Which medication improves congestive symptomsof heart failure most rapidly?a. Nitratesb. Beta-blockersc. Diureticsd. Amiodarone

25. An ideal drug (or drug combination) for thetreatment of acutely decompensated heartfailure would:a. reduce preload.b. enhance left ventricular function.c. maintain or improve myocardial oxygen balance.d. all of the above.

26. ACE inhibitors are contraindicated in heart failurepatients with which of the following conditions?a. Peanut allergyb. Hyperkalemiac. Hypokalemiad. Current menses

27. Which of the following excludes a patient from atrial of CPAP?a. Diaphoresisb. Renal failurec. Left ventricular hypertrophy on ECGd. Severe agitation

28. Which of the following indicators has beenshown to correlate with left ventricular overload,severity of clinical heart failure, and both short-and long-term cardiovascular mortality in heartfailure patients?a. ESRb. CRPc. BNPd. d-dimer ELISA

29. Which of the following is true?a. A normal ECG rules out left ventricular diastolic

dysfunction.b. Acute ST-segment elevation in a patient with

decompensated heart failure is a contraindica-tion for thrombolytic therapy.

c. Clinical findings usually lag behind chest x-rayfindings in heart failure patients.

d. Heart size may be normal in acute heart failure.

30. Cardiac enzymes:a. are not necessary if the ECG is normal.b. are always positive in the case of MI by the

time the patient is symptomatic.c. should be drawn on all patients with

heart failure.d. are indicated when the patient has

anginal-type pain or has unexplainedsudden-onset heart failure.


Class I• Always acceptable, safe• Definitely useful• Proven in both efficacy and

effectiveness

Level of Evidence:• One or more large prospective

studies are present (withrare exceptions)

• High-quality meta-analyses• Study results consistently

positive and compelling

Class II• Safe, acceptable• Probably useful

Level of Evidence:• Generally higher levels

of evidence• Non-randomized or retrospec-

tive studies: historic, cohort, orcase-control studies

• Less robust RCTs• Results consistently positive

Class III• May be acceptable• Possibly useful• Considered optional or

alternative treatments

Level of Evidence:• Generally lower or intermedi-

ate levels of evidence

• Case series, animal studies,consensus panels

• Occasionally positive results

Indeterminate• Continuing area of research• No recommendations until

further research

Level of Evidence:• Evidence not available• Higher studies in progress• Results inconsistent,

contradictory• Results not compelling

Significantly modified from: TheEmergency Cardiovascular CareCommittees of the American HeartAssociation and representativesfrom the resuscitation councils ofILCOR: How to Develop Evidence-Based Guidelines for EmergencyCardiac Care: Quality of Evidenceand Classes of Recommendations;also: Anonymous. Guidelines forcardiopulmonary resuscitation andemergency cardiac care. Emer-gency Cardiac Care Committee andSubcommittees, American HeartAssociation. Part IX. Ensuringeffectiveness of community-wideemergency cardiac care. JAMA1992;268(16):2289-2295.

Class Of Evidence Definitions

Each action in the clinical pathways section of EmergencyMedicine Practice receives an alpha-numerical score based onthe following definitions.

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Physician CME InformationThis CME enduring material is sponsored by Mount Sinai School ofMedicine and has been planned and implemented in accordance withthe Essentials and Standards of the Accreditation Council for ContinuingMedical Education. Credit may be obtained by reading each issue andcompleting the post-tests administered in December and June.

Target Audience: This enduring material is designed for emergencymedicine physicians.

Needs Assessment: The need for this educational activity wasdetermined by a survey of medical staff, including the editorial boardof this publication; review of morbidity and mortality data from theCDC, AHA, NCHS, and ACEP; and evaluation of prior activities foremergency physicians.

Date of Original Release: This issue of Emergency MedicinePractice was published February 1, 2002. This activity is eligible forCME credit through February 1, 2005. The latest review of this materialwas January 18, 2002.

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Faculty Disclosure: In compliance with all ACCME Essentials, Standards,and Guidelines, all faculty for this CME activity were asked to completea full disclosure statement. The information received is as follows: Dr.Kosowsky, Dr. Kobayashi, Dr. Fesmire, and Dr. Rosko report nosignificant financial interest or other relationship with themanufacturer(s) of any commercial product(s) discussed in thiseducational presentation.

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Earning Credit: Physicians with current and valid licenses in the UnitedStates, who read all CME articles during each Emergency MedicinePractice six-month testing period, complete the CME post-test andEvaluation Form distributed with the December and June issues, andreturn it according to the published instructions are eligible for up to4 hours of Category 1 credit toward the AMA Physician’s RecognitionAward (PRA) for each issue. You must complete both the post-test andCME Evaluation Form to receive credit. Results will be keptconfidential. CME certificates will be mailed to each participantscoring higher than 70% at the end of the six-month testing period.

31. Which of the following statements regarding heartfailure is true?a. Morphine’s main effect is through its direct

effect on cardiac contractility.b. Morphine may cause respiratory depression and

increase the incidence of intubation.c. Diuretics are more important than nitrates in

managing acute respiratory distress.d. Furosemide has no vasodilating properties.

32. Which of the following is true about ACE inhibitors?a. They reduce both preload and afterload.b. They promote sodium retention.c. They increase sympathetic stimulation.d. They decrease left ventricular function.

Acutely Decompensated Heart Failure

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